Structural studies of p53 inactivation by DNA-contact mutations and its rescue by suppressor mutations via alternative protein–DNA interactions

A p53 hot-spot mutation found frequently in human cancer is the replacement of R273 by histidine or cysteine residues resulting in p53 loss of function as a tumor suppressor. These mutants can be reactivated by the incorporation of second-site suppressor mutations. Here, we present high-resolution c...

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Detalles Bibliográficos
Autores principales: Eldar, Amir, Rozenberg, Haim, Diskin-Posner, Yael, Rohs, Remo, Shakked, Zippora
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2013
Materias:
Structural Biology
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3794590/
https://www.ncbi.nlm.nih.gov/pubmed/23863845
http://dx.doi.org/10.1093/nar/gkt630

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3794590/
https://www.ncbi.nlm.nih.gov/pubmed/23863845
http://dx.doi.org/10.1093/nar/gkt630

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